| Project/Area Number |
20592127
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Emergency medicine
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| Research Institution | Keio University |
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Principal Investigator |
FUJISHIM Seitaro Keio University, 医学部, 准教授 (00173419)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAKI Masaru 慶應義塾大学, 医学部, 助教 (60365400)
SEKINE Kazuhiko 慶應義塾大学, 医学部, 共同研究員 (90296715)
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| Co-Investigator(Renkei-kenkyūsha) |
NAKANO Yasushi 慶應義塾大学, 医学部, 助教 (90528225)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | CCR4 / interleukin-18 / SIRS / interleukin-17 / Interleukin-18 / 急性肺損傷 / Interleukin-17 / ARDS / IL-18 / ALI |
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| Research Abstract |
We hypothesized that abnormal paracellular environmental changes under severe insults induce overwhelming inflammation, hypersensitivity to infection, and imnuno-suppression, and used mice models of systemic inflammatory response syndrome and acute lung injury (ALI), as well as in vitro cell culture systems. We found that decrease in IL-18 levels induced changes in numerous genes in vitro, and in vivo supplementation of IL-18 resulted in anti-inflammatory effects in animal models. Furthermore, using a mouse model of ALI, we found that lack of IL-17 aggravated inflammation, suggesting new roles of IL-17.
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